Pitavastatin
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| Pitavastatin
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| Systematic (IUPAC) name | |
| (E)-7-[2-cyclopropyl-4-(4-fluorophenyl) quinolin-3-yl]-3,5-dihydroxy-hept-6-enoic acid | |
| Identifiers | |
| CAS number | |
| ATC code | C10 |
| PubChem | |
| Chemical data | |
| Formula | C25H24FNO4 |
| Mol. mass | 421.461 |
| Pharmacokinetic data | |
| Bioavailability | 60% |
| Protein binding | 96% |
| Metabolism | hepatic |
| Half life | 11 hours |
| Excretion | biliary |
| Therapeutic considerations | |
| Pregnancy cat. |
X |
| Legal status |
prescription |
| Routes | oral tablets 1 & 2 mg |
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Pitavastatin (usually as a calcium salt) is a novel member of the medication class of statins.[1] Like the other statins, it is an inhibitor of HMG-CoA reductase, the enzyme that catalyses the first step of cholesterol synthesis. It has been available in Japan since 2003, and is being marketed under licence in South Korea and in India.[1] It is likely that pitavastatin will be approved for use in hypercholesterolaemia (elevated levels of cholesterol in the blood) and for the prevention of cardiovascular disease outside South and Southeast Asia as well.[1]
History
Pitavastatin (previously known as itavastatin, itabavastin, nisvastatin, NK-104 or NKS-104) was discovered in Japan by Nissan Chemical Industries, Ltd. and developed further by Kowa Pharmaceuticals, Tokyo.[1]
Uses
Like the other statins, pitavastatin is indicated for hypercholesterolaemia (elevated cholesterol) and for the prevention of cardiovascular disease.
Side-effects
Common statin-related side-effects (headaches, stomach upset, abnormal liver function tests and muscle cramps) were similar to other statins.[1]
Metabolism and interactions
Most statins are metabolised in part by one or more hepatic cytochrome P450 enzymes, leading to an increased potential for drug interactions and problems with certain foods (such as grapefruit juice). Pitavastatin appears to be a substrate of CYP2C9, and not CYP3A4 (which is a common source of interactions in other statins).[1]
References
External links
Lipid modifying agents (C10) | |
|---|---|
| Statins | Atorvastatin • Cerivastatin • Fluvastatin • Lovastatin • Mevastatin • Pitavastatin • Pravastatin • Rosuvastatin • Simvastatin |
| Fibrates | Clofibrate • Bezafibrate • Aluminium clofibrate • Gemfibrozil • Fenofibrate • Simfibrate • Ronifibrate • Ciprofibrate • Etofibrate • Clofibride |
| Bile acid sequestrants | Colestyramine • Colestipol • Colextran • Colesevelam |
| Niacin and derivatives | Niceritrol • Niacin • Nicofuranose • Aluminium nicotinate • Nicotinyl alcohol • Acipimox |
| Other | Dextrothyroxine • Probucol • Tiadenol • Benfluorex • Meglutol • Omega-3-triglycerides • Magnesium pyridoxal 5-phosphate glutamate • Policosanol • Ezetimibe |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
